General Discussion: Environmental Toxicants

1984 ◽  
pp. 81-90
Author(s):  
A. M. Chakrabarty ◽  
Gilbert S. Omenn ◽  
Simon Silver ◽  
Andrew Weightman
Keyword(s):  
Environmental Toxicants

Troubling Figures

2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Logan Natalie O'Laughlin
Keyword(s):  
Critical Discourse Analysis ◽  
Science Studies ◽  
Critical Discourse ◽  
People Of Color ◽  
Careful Examination ◽  
Environmental Toxicants ◽  
Environmental Racism ◽  
Feminist Science Studies ◽  
Feminist Science ◽  
Do So

This essay examines the figure of the pesticide-exposed intersex frog, a canary in the coal mine for public endocrinological health. Through feminist science studies and critical discourse analysis, I explore the fields that bring this figure into being (endocrinology, toxicology, and pest science) and the colonial and racial logics that shape these fields. In so doing, I attend to the multiple nonhuman actors shaping this figure, including the pesky weeds and insects who prompt pesticides’ very existence, “male” frogs who function as test subjects, and systemic environmental racism that disproportionately exposes people of color to environmental toxicants. I encourage careful examination of galvanizing environmental figures like this toxic intersex frog and I offer a method to do so.

Mechanistic Overview of Immune Modulatory Effects of Environmental Toxicants

2015 ◽  
Vol 13 (6) ◽  
pp. 382-386 ◽  
Author(s):  
Haji Bahadar ◽  
Mohammad Abdollahi ◽  
Faheem Maqbool ◽  
Maryam Baeeri ◽  
Kamal Niaz
Keyword(s):  
Environmental Toxicants

scholarly journals A predictive in vitro risk assessment platform for pro-arrhythmic toxicity using human 3D cardiac microtissues

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Celinda M. Kofron ◽  
Tae Yun Kim ◽  
Fabiola Munarin ◽  
Arvin H. Soepriatna ◽  
Rajeev J. Kant ◽  
...  
Keyword(s):  
Risk Assessment ◽  
Action Potentials ◽  
Induced Pluripotent Stem Cell ◽  
Human Action ◽  
Environmental Toxicants ◽  
Pharmaceutical Drugs ◽  
Industrial Chemicals ◽  
Endocrine Disrupting Chemical

AbstractCardiotoxicity of pharmaceutical drugs, industrial chemicals, and environmental toxicants can be severe, even life threatening, which necessitates a thorough evaluation of the human response to chemical compounds. Predicting risks for arrhythmia and sudden cardiac death accurately is critical for defining safety profiles. Currently available approaches have limitations including a focus on single select ion channels, the use of non-human species in vitro and in vivo, and limited direct physiological translation. We have advanced the robustness and reproducibility of in vitro platforms for assessing pro-arrhythmic cardiotoxicity using human induced pluripotent stem cell-derived cardiomyocytes and human cardiac fibroblasts in 3-dimensional microtissues. Using automated algorithms and statistical analyses of eight comprehensive evaluation metrics of cardiac action potentials, we demonstrate that tissue-engineered human cardiac microtissues respond appropriately to physiological stimuli and effectively differentiate between high-risk and low-risk compounds exhibiting blockade of the hERG channel (E4031 and ranolazine, respectively). Further, we show that the environmental endocrine disrupting chemical bisphenol-A (BPA) causes acute and sensitive disruption of human action potentials in the nanomolar range. Thus, this novel human 3D in vitro pro-arrhythmic risk assessment platform addresses critical needs in cardiotoxicity testing for both environmental and pharmaceutical compounds and can be leveraged to establish safe human exposure levels.

Dysregulation of G protein-coupled receptors in the intestine by nanoplastic exposure in Caenorhabditis elegans

2021 ◽  
Author(s):  
Yunhan Yang ◽  
Qiuli Wu ◽  
Dayong Wang
Keyword(s):  
Caenorhabditis Elegans ◽  
G Protein ◽  
G Protein Coupled Receptors ◽  
Environmental Toxicants ◽  
G Protein Coupled

After the uptake, the environmental toxicants may cause the toxicity on organisms by activating or inhibiting certain G protein-coupled receptors (GPCRs). Nevertheless, the roles of GPCRs in mediating the response...

scholarly journals Cytotoxic Effects of N,N-Diethyl-Meta-Toluamide (DEET) on Sinonasal Epithelia

OTO Open ◽  
2021 ◽  
Vol 5 (2) ◽  
pp. 2473974X2110092
Author(s):  
Jivianne T. Lee ◽  
Saroj Basak
Keyword(s):  
Cell Viability ◽  
Chronic Rhinosinusitis ◽  
Morphological Changes ◽  
Environmental Toxicants ◽  
Cytotoxic Effects ◽  
Airborne Pollutants ◽  
Cell Monitoring ◽  
History Of ◽  
And Control ◽  
Dose Dependent

Although the etiology of chronic rhinosinusitis remains unknown, environmental factors including airborne pollutants and toxicants are postulated to contribute to its pathogenesis. However, the precise pathomechanisms with which environmental toxicants may contribute to chronic rhinosinusitis are not fully understood. The purpose of this pilot study is to examine the cytotoxic effects of N,N-diethyl- meta-toluamide (DEET), a commonly used pesticide, on sinonasal epithelial cells (SNECs). Sinus mucosa was obtained from 3 subjects without a history of chronic rhinosinusitis. Cultured SNECs were exposed to various concentrations of DEET (0-5 mM) for 6 days. Cell viability, proliferation, and morphologic changes were assessed using the MTT colorimetric dye assay and the Incucyte Live Cell Monitoring System. Statistically significant dose-dependent reduction in cell viability and proliferation was observed between exposure and control groups ( P < .05) at all concentrations tested. Dose-dependent cellular morphological changes were also seen. These findings indicate that DEET exposure induces dose-dependent cytotoxicity in sinonasal epithelia.

scholarly journals Correction: Phosphatidylcholine Specific PLC-Induced Dysregulation of Gap Junctions, a Robust Cellular Response to Environmental Toxicants, and Prevention by Resveratrol in a Rat Liver Cell Model

PLoS ONE ◽  
2015 ◽  
Vol 10 (9) ◽  
pp. e0137599
Author(s):  
Faiz Ahmed Raza ◽  
Shafiq ur Rehman ◽  
Ruqyya Khalid ◽  
Jameel Ahmad ◽  
Sajjad Ashraf ◽  
...  
Keyword(s):  
Gap Junctions ◽  
Rat Liver ◽  
Liver Cell ◽  
Cellular Response ◽  
Cell Model ◽  
Environmental Toxicants ◽  
Liver Cell Model

Children’s Behavior and Physiology and How It Affects Exposure to Environmental Contaminants

PEDIATRICS ◽  
2004 ◽  
Vol 113 (Supplement_3) ◽  
pp. 996-1006
Author(s):  
Jacqueline Moya ◽  
Cynthia F. Bearer ◽  
Ruth A. Etzel
Keyword(s):  
Surface Area ◽  
Lead Poisoning ◽  
Environmental Contaminants ◽  
Activity Level ◽  
Second Hand Smoke ◽  
Environmental Toxicants ◽  
Soil Ingestion ◽  
Adults And Children ◽  
Food And Water Intake ◽  
Noxious Effect

Infant, child, and adolescent exposures to environmental toxicants are different from those of adults because of differences in behavior and physiology. Because of these differences, there is the potential for quantitatively different exposures at various stages of development. Pediatricians are well aware of these behavioral and physiologic differences from a clinical standpoint—namely, food and water intake, soil ingestion, mouthing behavior, inhalation physiology, and activity level—as they relate to the ratio of these parameters between the adult and the child when considering weight and surface area. Pediatricians recognized the importance of pica as a cause of lead poisoning, the noxious effect of second-hand smoke, and the greater propensity for addiction during the adolescent years. For determining the differences in impact of many environmental toxicants between adults and children, research is needed to document where and whether these differences result in deleterious effects.

scholarly journals A Human Relevant Defined Mixture of Persistent Organic Pollutants (POPs) Affects In Vitro Secretion of Glucagon-Like Peptide 1 (GLP-1), but Does Not Affect Translocation of Its Receptor

2019 ◽  
Vol 172 (2) ◽  
pp. 359-367 ◽  
Author(s):  
Maeve Shannon ◽  
Yuling Xie ◽  
Steven Verhaegen ◽  
Jodie Wilson ◽  
Hanne F Berntsen ◽  
...  
Keyword(s):  
Organic Pollutants ◽  
Persistent Organic Pollutants ◽  
Complex Mixture ◽  
Blood Levels ◽  
Environmental Toxicants ◽  
Blood Concentrations ◽  
Total Mixture ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Abstract Environmental exposure to persistent organic pollutants (POPs) has been suggested as a contributing factor for the increased rate of type 2 diabetes and obesity. A complex mixture of 29 POPs (Total mixture), based on human blood concentrations, was used to expose a glucagon-like peptide 1 (GLP-1) secreting enteroendocrine cell line (pGIP/neo: STC-1) in vitro for 3 and 24 h. Significant increases of GLP-1 occurred when cells were exposed to the Total mixture at ×500 blood levels. Six sub-mixtures representing chlorinated (Cl), brominated (Br), and perfluorinated chemicals (PFAA), and their combinations (Cl + Br, Cl + PFAA, Br + PFAA) were also tested at ×500. Secretion levels seen for these remained lower than the Total mixture, and the Br mixture had no effect. After 24 h, increased secretion was seen with all mixtures at ×1 blood levels. Cytotoxicity was present for ×100 and ×500 blood levels. When tested in a GLP-1 receptor translocation assay (U2OS-GLP1R-EGFP), neither agonistic nor antagonist effects on receptor internalization were seen for any of the mixtures. We conclude individual classes of POPs, alone or in combination, can affect GLP-1 secretion and may contribute as a molecular mechanism linking environmental toxicants and diabetes.

scholarly journals Chemopreventive Agents Attenuate Rapid Inhibition of Gap Junctional Intercellular Communication Induced by Environmental Toxicants

2016 ◽  
Vol 68 (5) ◽  
pp. 827-837 ◽  
Author(s):  
Pavel Babica ◽  
Lucie Čtveráčková ◽  
Zuzana Lenčešová ◽  
James E. Trosko ◽  
Brad L. Upham
Keyword(s):  
Intercellular Communication ◽  
Environmental Toxicants ◽  
Gap Junctional Intercellular Communication ◽  
Chemopreventive Agents ◽  
Gap Junctional
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